In humans, obesity and sterile inflammation are recognized as critical risk factors of atrial fibrillation (AF) pathogenesis, which is a leading risk factor of stroke. It is currently unknown what associative molecular mechanisms occur, involving these factors, to perpetuate AF pathophysiology. Using genetically adaptable mouse models and other biomedical techniques, our studies have shown a correlation between NLRP3 activation and AF incidence. Moving forward, this research intends to characterize how obesity caused by calorie-intensive Western diet exposure, can influence NLRP3 inflammasome activation to promote downstream mechanisms that drive AF development. By confirming a link between obesity instance and NLRP3 induced AF, we can potentially establish accurate targets for therapy to attenuate the AF arrhythmia and associated downstream effects.